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Ca 2+ /calmodulin is involved in growth factor‐induced retinoblastoma gene product phosphorylation in human vascular endothelial cells
Author(s) -
Takuwa Noriko,
Zhou Wei,
Kumada Mamoru,
Takuwa Yoh
Publication year - 1992
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(92)80993-q
Subject(s) - calmodulin , phosphorylation , vascular endothelial growth factor , vascular endothelial growth factor b , gene , chemistry , gene product , vascular endothelial growth factor a , retinoblastoma , vascular endothelial growth factor c , microbiology and biotechnology , cancer research , vegf receptors , biology , gene expression , biochemistry , enzyme
In human vascular endothelial cells, both growth factor‐induced DNA synthesis and retinoblastoma gene product (RB) phosphorylation are absolutely dependent on extracellular Ca 2+ , and are potently inhibited by an active calmodulin antagonits, W‐7, but not an inactive analogue, W‐12. A reduction in the extracellular Ca 2+ or an addition of W‐7 as late as 8 h after growth factor stimulation still inhibits both RB phosphorylation and DNA synthesis to the full extent. However, once RB phosphorylation occurs 12–16 h after addition of the growth factors, it is not reversed by subsequent Ca 2+ reduction or W‐7. These results suggest the existence of a Ca 2+ /calmodulin‐dependent process relatively late in the mitogenic signalling cascade, at a step proximal to RB phosphorylation reaction itself.